Scott J. Russo

This study examines how dopamine availability and immune activation interact to influence anhedonia severity in youth with depression.

The paper identifies the CSF YWHAG:NPTX2 ratio as a biomarker for predicting clinical severity and phenoconversion in FTLD, showing strong correlation with disease progression and improved trial design potential.

The paper identifies synaptic bioenergetic remodeling in the mPFC after heroin abstinence, but not cocaine, and links it to relapse vulnerability.

The paper develops a method to study endogenous protein complexes in brain tissue and finds mGluR2/3 heterodimers are abundant in specific human brain regions and associated with depression.

The paper identifies a shared transcriptional network in the nucleus accumbens that supports stress resilience in both sexes and shows causal effects of hub genes.

This study shows that early life stress causes sex-specific H3K27me1 accumulation in the prefrontal cortex, leading to long-term behavioral and cognitive effects in mice.

The paper identifies sex-specific mesoscale co-activation modules in aggression-related brain networks using c-Fos imaging and network analysis in mice.

This study shows LINC00473 in mPFC modulates sex-dependent change-of-mind behavior in mice by affecting value caching and mistake weighting in a neuroeconomic task.

The paper identifies ZBTB7A as a key regulator of MDD-specific chromatin signatures and astrocyte-mediated stress vulnerability in the orbitofrontal cortex.

This study identifies astrocyte-derived extracellular matrix proteins, particularly SPARC, as regulators of synapse remodeling in stress-induced depression.

The paper identifies dopaminylated proteins in the brain, including γCaMKII, and shows its role in synaptic-to-nuclear signaling and memory formation.

This study identifies H3K27me1 as a chromatin scar that mediates lifelong stress susceptibility through its role in altering gene expression in the nucleus accumbens.

The paper identifies sex-specific regulation of stress susceptibility by the astrocytic gene Htra1 in mice and humans, showing differential effects on neuronal signaling and ECM integrity.

The paper investigates genetic and sex differences in stress and morphine responses across mouse strains and their progeny, finding genetic influences on stress vulnerability and morphine sensitivity.

The paper identifies distinct transcriptional profiles in striatal ensembles activated during initial vs. repeated cocaine exposure, revealing differences in neuronal recruitment and memory retrieval mechanisms.

The paper investigates how serotonin modifies histone H3K4me3Q5ser dynamics in the dorsal raphe nucleus under stress and antidepressant exposure, showing its role in gene expression and behavior.

This study identifies RXR as a key regulator of drug reward sensitivity in the nucleus accumbens through transcriptional control of neuronal excitability in mice.

The paper shows that editing a specific brain circuit in mice reduces violent behavior without affecting non-aggressive social interactions.

The paper investigates how CREB function in specific brain regions influences distinct forms of regret related to resilience and susceptibility to chronic stress in mice.

The paper investigates sex differences in reactive and appetitive aggression in mice using behavioral tests, revealing distinct patterns between males and females.

The paper shows that social rank and history of winning influence stress susceptibility in mice, with dominance conferring resilience and subordination increasing susceptibility.

This study shows cocaine affects mitochondrial dynamics in neurons by regulating Egr3 transcription of mitochondrial-related genes, with distinct effects in D1-MSNs and D2-MSNs.

This study shows that LRRK2-G2019S mutation alters behavioral and synaptic responses to acute social stress in mice, suggesting impaired adaptive plasticity in neural circuits linked to psychopathology.

This study shows orexin signaling in GABAergic lateral habenula neurons promotes aggression and conditioned place preference, suggesting a potential therapeutic target for reducing aggressive behaviors.

This study identifies WT1 as a transcriptional repressor that decreases memory strength and promotes memory flexibility by regulating synaptic plasticity and learning outcomes.

This study shows that CSF-1 signaling is essential for cerebellar microglia identity and function, and its disruption causes motor and social behavior defects.